Our findings about the slower propagation of EA and the possible implication of glutamate receptors could shed light on the implication of the gene LIS1 on complex electrical responses that are generated by cortical circuits; however, given that human lissencephaly is strongly determined by cortical structural abnormalities (and our model lacks those abnormalities) it is difficult to relate our findings to those pathophysiological mechanisms underlying the clinical symptoms of lissencephaly. This evidence concerns the gene PAFAH1B1 and lissencephaly spectrum disorders.